Overview
Clinical Meaning
PCOS pathophysiology centers on disrupted hypothalamic GnRH pulsatility producing a persistently elevated LH:FSH ratio.
AGPCNP
AGPCNP
PCOS pathophysiology centers on disrupted hypothalamic GnRH pulsatility producing a persistently elevated LH:FSH ratio. Elevated LH overstimulates ovarian thecal cells to produce excess androgens (testosterone, androstenedione), while relatively low FSH fails to support follicular maturation past the antral stage, causing follicular arrest and anovulation. Concurrently, hyperinsulinemia from peripheral insulin resistance directly stimulates thecal androgen production via insulin and IGF-1 receptors, and suppresses hepatic SHBG synthesis, increasing free testosterone bioavailability. This creates a self-perpetuating cycle: hyperandrogenism disrupts follicular development, preventing the estrogen surge needed for ovulation, while adipose tissue aromatizes excess androgens to estrone, providing continuous (rather than cyclic) estrogen that further suppresses FSH through negative feedback.
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